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Piezo2 senses airway stretch and mediates lung inflation-induced apnoea

机译：Piezo2感知气道舒展并介导肺膨胀引起的呼吸暂停

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摘要

Respiratory dysfunction is a notorious cause of perinatal mortality in infants and sleep apnoea in adults, but the mechanisms of respiratory control are not clearly understood. Mechanical signals transduced by airway-innervating sensory neurons control respiration; however, the physiological significance and molecular mechanisms of these signals remain obscured. Here we show that global and sensory neuron-specific ablation of the mechanically activated ion channel Piezo2 causes respiratory distress and death in newborn mice. Optogenetic activation of Piezo2(+) vagal sensory neurons causes apnoea in adult mice. Moreover, induced ablation of Piezo2 in sensory neurons of adult mice causes decreased neuronal responses to lung inflation, an impaired Hering-Breuer mechanoreflex, and increased tidal volume under normal conditions. These phenotypes are reproduced in mice lacking Piezo2 in the nodose ganglion. Our data suggest that Piezo2 is an airway stretch sensor and that Piezo2-mediated mechanotransduction within various airway-innervating sensory neurons is critical for establishing efficient respiration at birth and maintaining normal breathing in adults.
机译：呼吸功能障碍是婴儿围产期死亡和成人睡眠呼吸暂停的臭名昭著的原因，但是呼吸控制的机制尚不清楚。气道内感觉神经元转导的机械信号控制呼吸。但是，这些信号的生理意义和分子机制仍然不清楚。在这里，我们显示机械激活的离子通道Piezo2的整体和感觉神经元特异性消融导致新生小鼠呼吸窘迫和死亡。 Piezo2（+）迷走神经感觉神经元的光遗传学激活导致成年小鼠呼吸暂停。此外，在正常情况下，成年小鼠感觉神经元中Piezo2的诱导消融导致神经元对肺膨胀的反应减少，Hering-Breuer机械反射减弱以及潮气量增加。这些表型在结节神经节中缺乏Piezo2的小鼠中复制。我们的数据表明，Piezo2是一种气道舒张传感器，并且在各种气道激活感觉神经元内，Piezo2介导的机械转导对于在出生时建立有效的呼吸和维持成年人的正常呼吸至关重要。

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  • 来源
    《Nature》 |2017年第7636期|176-181|共6页
  • 作者

    Nonomura Keiko; Woo Seung-Hyun; Chang Rui B.; Gillich Astrid; Qiu Zhaozhu; Francisco Allain G.; Ranade Sanjeev S.; Liberles Stephen D.; Patapoutian Ardem;

  • 作者单位

    Scripps Res Inst, Dorris Neurosci Ctr, Howard Hughes Med Inst, Mol & Cellular Neurosci, La Jolla, CA 92037 USA;

    Scripps Res Inst, Dorris Neurosci Ctr, Howard Hughes Med Inst, Mol & Cellular Neurosci, La Jolla, CA 92037 USA;

    Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA;

    Stanford Univ, Sch Med, Howard Hughes Med Inst, Dept Biochem, Stanford, CA 94305 USA;

    Scripps Res Inst, Dorris Neurosci Ctr, Howard Hughes Med Inst, Mol & Cellular Neurosci, La Jolla, CA 92037 USA|Novartis Res Fdn, Genom Inst, San Diego, CA 92121 USA|Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA|Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA;

    Scripps Res Inst, Dorris Neurosci Ctr, Howard Hughes Med Inst, Mol & Cellular Neurosci, La Jolla, CA 92037 USA;

    Scripps Res Inst, Dorris Neurosci Ctr, Howard Hughes Med Inst, Mol & Cellular Neurosci, La Jolla, CA 92037 USA|Gladstone Inst, San Francisco, CA 94158 USA;

    Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA;

    Scripps Res Inst, Dorris Neurosci Ctr, Howard Hughes Med Inst, Mol & Cellular Neurosci, La Jolla, CA 92037 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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